OP / Paget / Bone diseases Flashcards
1
Q
** Modifiable RF for OP**
A
-Low Ca or vit D
-Sedentary
-Smoking, Caffeine/Alcohol (>2/d)
-Drugs: GC, Lithium, Heparin, AED, Aromatase inhib, Tamoxifen,
2
Q
** Nonmodifiable RF for OP**
A
- Age
-Race (caucasian, asian)
-Female
-Early menopause
-BMD - Slender build
-Positive family hip # hx
-Comorbid: RA, hyperPTH, thyroid, hypogonad, celiac, bypass, Freq falls
3
Q
OP Diagnosis
A
Fragility Fracture = OP
Low BMD:
-T score <-2.5 in pt >50 w/o fracture; OR
-Z score <2 for premenopausal woman or man <50
High Frax: >20% for major OP # or >3% hip #
4
Q
** OP physical exam findings**
A
-Weight <60kg
-BMI <20
-Height loss 2cm+ prospective, 6cm+ historical
-Rib pelvis <2fingerbreadths
-Wall to occiput >5cm
-Tooth count <20
-Kyphosis
-Arm height span >5cm
-Grip strength
-Hand skinfold thickness
5
Q
** How to detect vertebral # **
– Clinically
– Investigations
A
Clinically: ht loss 6cm, dorsal kyphosis, occiput to wall, rib to pelvis
-XR (vertebral body height of at least 20% or 4mm height reduction) or DXA
6
Q
Indications for BMD testing
A
- > 50 with 2 RF, >65 with 1, >70
-Estrogen deficiency with 1 RF for OP
-Vertebral deformity, fracture, or osteopenia on XR
-Hyperparathyroid
-Steroids: >5mg x3mo
-Monitoring response to OP meds
7
Q
What is Z score and what does it tell you
A
Zscore = adjusted for age
-Tells you if there’s something other than age or menopause causing low BMD
8
Q
** Low BMD DDx**
A
-Cushings, Hypogonadism, Hyperthyroid/PTH
-RA, SLE, Ank Spond
-Eating/exercise disorder
-Meds, Alcoholism
-Renal failure, RTA, chronic hypoNa, idiopathic hypercalciuria, MM
-IBD, Celiac, PBC, gastrectomy/bypass
-Osteomalacia, osteogenesis imperfecta, ehlers danlos
9
Q
** Meds causing low BMD **
A
Steroids,
Lithium, SSRI, Antipsychotic
-AEDs,
-Excess synthroid
-Tamoxifen, Aromatase inhib,
-Cyclosporin,
-Chemo,
-Leuprolide,
-Heparin
10
Q
Low BMD Labs
A
- Ca, albumin, PO4
-PTH, TSH
-Vitamin D
-Cr
-ALP
-Testosterone
-Urine calcium, Na, Cr
-SPEP (if >50yo and abnormal CBC)
-Celiac antibody
11
Q
RF for freq falls
A
-Frailty, lower extremity disability
-Meds (sedatives)
-Impaired vision and cognition
-Obstacles in the home
-Previous fall
12
Q
Nonpharm Tx OP
A
Ca
-Vit D
-Stop smoking
-Exercise
13
Q
** GIOP pathophysiology**
A
-OB: apoptosis and reduced development (decr Wnt)
-Osteocytes: apoptosis (via caspase 3)
-OC: increased due to decreased sex steroid (incr RANKL) and osteoprotegerin (inhib of resorption)
-Ca: increase renal excretion, decrease GI absorption
-Muscle mass decreases (falls risk)
14
Q
** CAROC components**
A
- BMD
-Age
-Gender
-Previous fragility fracture >40 or prolonged steroids (>7.5mg/d x3mo) (increase risk class by 1)
-Vertebral/hip fracture or >1 fragility # = high risk
15
Q
** FRAX components**
A
- Age
- Sex
- Previous fragility #
- BMI
- Parental hip fracture
- Rheumatoid arthritis
- 2ndary conditions that contribute to bone loss (T1DM, osteogenesis imperfecta, untreated hyperthyroid, hypogonad or premature menopause <45 years, chronic malnutrition, malabsorption, chronic liver disease)
- Current smoking
- Alcohol intake (3+/day)
- Femoral neck BMD
- Country of current living
- Steroid exposure (current or >5mg x3 mo)
16
Q
FRAX risk cutoff
A
Low: <10% MOP, <1% hip #
-Med: 10-19% MOP, 1-3% hip #
-High: >20% MOP, >3% hip #
17
Q
When to treat GIOP
A
Over 40:
-Low risk FRAX + pred 5-7.5mg/d >3mo
-Med risk FRAX + pred >2.5mg/d
-High risk
-
-Under 40:
-Low risk: if >10% BMD loss in 1 yr or expected >5g pred in 1 year
-Medium and high risk
18
Q
Pregnancy OP Med Considerations
A
Teriparatide if preg anticipated
-Risdedronate (least fetal tox)
-Prolia CONTRAINDICATED
19
Q
** Vit D metabolism**
A
Skin makes D3 (cholecalciferol) from sun
-Diet intake D2 (ergocalciferol) and D3
-Both converted to 25-OH-vit D in liver
-Converted to 1,25-OH2-Vit D in kidney by 1 alpha hydroxylase (induced by PTH and hypophosphatemia; inhib by fibroblast growth factor 23)
-1,25OH2 vit D binds intestinal vit D receptor for Ca/PO4 absorption
20
Q
Osteomalacia / Rickets clinical /imaging features
A
Soft bones from impaired mineralization
- Pain/deformity long bones and pelvis
- XR: pseudofractures
21
Q
Vit D def osteomalacia lab results
A
Low Ca, PO4, Vit D, 24h urine Ca
High PTH and ALP
22
Q
Renal PO4 wasting osteomalacia labs
A
Low PO4, high urine PO4,
High ALP,
Normal/inappropriately low Vit D for ALP lvls
23
Q
Rickets congenital causes
A
X-linked Hypophosphatemic → increased FGF23 → phosphaturic and decrease intestinal absorption of vit D
-Congenital 1 alpha hydroxylase def
-Congenital vit D resistance
24
Q
** Osteomalacia causes**
A
Vit D deficiency:
- Low PO intake, insuff sunlight, malabsorption, pancreatic insuff,
- Liver/renal dz → insuff vit D conversion,
- Drugs (AED, anti TB, HAART)
HypoPO4:
- Low PO intake
- PO4 binding antacid,
- Excess renal loss , Fanconi,
-Hypophosphatasia - from ALP gene mutation =can’t break down PP (inhibitor of mineralization)
Inhibitors of mineralization:
-Bisphosphonate,
-Aluminum,
-Fluoride
Oncogenic osteomalacia
-FGF23 secreting tumor - inhib PO4 transport and 1-a-hydroxylase enzyme in kidney
25
Rickets manifestations (NOT in osteomalacia)
-Widened cranial sutures
-Growth retardation
-XR: widened metaphyses and growth plates, thin cortex, sparse trabeculae
26
Ricketts/osteomalacia Tx
Vit D deficiency/resistance or malabsorption: → Vitamin D
Renal disease, hypophosphatemia, alpha hydroxylase deficiency: → calcitriol and oral PO4
27
Familial hyperphosphatemic tumoral calcinosis mutation and result
Inactivating mutation of FGF23 → painful ectopic calcification and elevated PO4 lvls
28
Osteogenesis imperfecta cause & Tx
Defective osteoblast fcn
-Tx: bisphosphonates in all by Type IV
29
Hypophosphatasia
-Cause
-Manifestations
-Tx
Cause: mutations inactivating alkaline phosphatase
-Manifestations: fetal demise, rickets, osteomalacia, #, OP, low ALP, high vitamin B5, high urine phosphoethanolamine
-Enzyme replacement, asfotase alpha
30
Osteopetrosis
-Cause
-Manifestations
-Tx
Defective osteoclast fcn → chalky fragile bone and osteosclerosis
-XR: generalized osteosclerosis
-Tx: Bone marrow transplant for normal osteoclasts + calcitriol to stimulate OC
31
** Paget’s pathophysiology**
Mutation or paramyxovirus infxn →
-LARGE OVERACTIVE OC → focal areas of excessive resorption (LYTIC phase)
-OB compensate to increase bone → DISORGANIZED weaker bone (MIXED lytic/sclerotic phase)
-Resorbed bone replaced w/ fibrous tissue and abN enlarged sclerotic bone (SCLEROTIC phase)
32
** Paget’s manifestations**
Bone pain (nocturnal, rest/activity)
-Deformities (tibial bowing, skull thickening) → neural compression
-Pseudofractures (transverse, chalkstick)
-Secondary OA
33
** Paget’s XR findings**
-Osteolysis w/ sclerotic changes (eg cotton wool skull, Osteoporosis circumscripta)
-Tam o Shanter sign
-Spine: picture frame sign, vertebral squaring,
-Coarse trabecular pattern
-Bone enlargement, Cortical thickening
-Blade of grass sign (wedge shaped resorption of long bones)
-Pelvic brim sign or Pelvic Ring
-Bowing deformities
-Pseudofractures (transverse linear radiolucency)
34
**Pagets DDX**
Chronic OM
-SAPHO
-Cancer: Osteosarcoma, vertebral hemangioma, lymphoma, mets (breast/PCa)
-Hyperostosis frontalis interna
-Fibrous dysplasia
35
Paget’s phases
Lytics
-Mixed lytic/sclerotic
-Sclerotic
36
Paget Dx vs monitoring
Dx: XR
-Extent of bone dz = bone scan
-ALP (high during osteoblastic)
-Bone specific ALP (BSAP) if liver dz falsely elevating ALP
37
**Tx Paget**
- Ca, Vit D
-Bisphosphonate (inhib OC): ZA = drug of choice
-Prolia (not approved indication)
-NSAID
-If neuropathic pain: gabapentin, pregabalin, amitriptyline
-Ortho consult: bone deformities, spinal canal stenosis, pseudofractures
-Canes, shoe lifts
38
**Paget when to treat**
-Symptoms: bone pain, radiculopathy, paraplegia, neural impingement, tinnitus, CHF, hearing deficit, H/A
-High risk sites: skull, spine, near major joints
-Pre-surgery near pagetic site (vascularity → blood loss)
-Hypercalcemia assoc’d w/ immobilization
39
**Paget complications categories **
MSK
-Neuro
-Vascular
-Cardiac
-Cancer
-Metabolic
40
**Paget MSK complications**
Bone pain,
-Deformities (bowing/bossing),
-Fractures
41
** Paget Neuro complications**
- Nerve entrapment (spinal nerves, cranial nerves)
- Deafness (auditory nerve)
-H/A, Vertigo, Tinnitus,
-Stroke (blood vessel compression)
- Basilar invagination
- Spinal stenosis
42
**Paget Vascular complications**
-Vascular steal syndrome (carotid blood flow to skull at brain's expense)
-Hyperthermia
43
**Paget Cardiac complications**
High output CHF,
-HTN,
-Cardiomegaly,
-Angina
44
**Paget Cancer complications**
Fibrosarcoma,
-Giant cell tumor,
-Osteosarcoma
45
**Paget Metabolic complications**
TOO MUCH CALCIUM (blood, urine, kidneys)
-Hypercalcemia,
-Hypercalciuria,
-Nephrocalcinosis
46
Bisphosphonate side fx
Osteonecrosis (esp in Ca and invasive dental procedure)
-AFF
-Nephrotox
-HypoCa
-Esophagitis, GERD
-Flu like illness
- Uveitis, keratitis, optic neuritis, orbital swelling
47
**Bisphosphonate mech of action**
- Pyrophosphate analog binds hydroxyapatite on bone
- Blocks farnesyl pyrophosphate synthase → prevent “ruffled border” formation and ability of OC to adhere to bone
- Also promote OC apoptosis
48
**Prolia mech of action**
- Human mAb against RANKL
- Prevents RANKL and RANK-receptor binding → inhib OC formation and resorption
49
**Teriparatide mech of action**
- PTH analog binding type 1 PTH R
-Increases GI and renal reabsorption of Ca
-Stimulates OB differentiation and survival
50
**Romosozumab mech of action**
- Humanized monoclonal AB (IgG2)
- Blocks sclerostin (usually inhib Wnt/Beta catenin signaling pathway)
- Thus more bone formation and less resorption
51
**AFF pathophys**
BP inhib OC and decrease remodelling → microdamage and stress fracture
52
**AFF RF**
-Small (low height/weight) asian female
-Steroids
-Long term bisphosphonate
-Low bone turnover marker (ALP)
53
**AFF manifestations**
Thigh pain
-Bird beak on lateral aspect
-Stress fracture
54
**AFF Ix**
-XR bilateral femurs - transverse/oblique#, thickened cortex, periosteal elevation, beaking of lateral cortex
-MRI/bone scan
55
**AFF Tx**
-Stop bisphosphonate
-Limited weightbearing
-Surgery: intramedullary nailing
-Teriparatide
56
Differentiate Paget bone pain vs OA
Lidocaine injection: helps OA not Paget
-Bisphosphonate: helps paget not OA
57
** Artifactual causes of higher BMD**
-- OA
-- DISH, AS
-- Vertebral #
-- Thalassemia
-- Vascular calcification
-- Abdo abscess
-- Gallstones, Kidney stones
-- Implants: silicone, surgical metalwork, pacemakers, catheters, bullets
-- Vertebroplasty and kyphoplasty
58
** True causes of higher BMD**
-SAPHO
-Chronic infective OM
-Acromegaly
-Osteopetrosis
-Tumors, Osteoblastoma, Mets (PCa)
-Hep C assoc’d osteosclerosis
-Myelofibrosis, Myelosclerosis, Mastocytosis
-Sclerosteosis
-Pagets
59
At risk areas for AVN
-Femoral/Humeral head
-Proximal tibia
-Carpal bones (scaphoid, lunate)
-Tarsal navicular, talus
-Metatarsals
-Vertebral body
60
AVN etiology and causes
Disruption of arterial blood supply
-- Trauma (hip dislocation, #, surgery)
-- Hypercoagulable: SS, Hgbopathy, thrombophilia, coagulopathy, fat emboli, SLE, APLA
-- BM hypertrophy/infiltration (Gaucher’s, leukemia, myeloproliferative d/o, STEROIDS)
-- BM tox/death (chemo, rads, thermal injury)
-- Peds: Legg calve perthes, slipped capital femoral epiphysis
-- DM, cushings, pancreatitis, OCP,
-- Cancer
-- Alcohol, Smoking
-- Idiopathic
-- Meds: Protease inhibitor for HIV, bisphosphonate
61
**Risk factors for jaw osteonecrosis**
-Age >65
-DM
-Smoking
-Steroid use
-Poor oral hygiene
-Invasive dental procedure (extraction,implants)
-High dose antiresorptive (bisphosphonate or prolia; NOT anabolics)
62
**Preventing jaw osteonecrosis**
Oral exam before starting BP
-Continue BP through dental if 4y and no RF
-Hold if >4y or concomitant steroids
63
** GC fx on AVN **
Indirect fx causing ischemia, 2/2:
-- Decreased angiogenesis
-- Vasoactive amine production
-- Increased intraosseous pressure from BM fat hypertrophy
PLUS
Same as GIOP (sex steroids, OPG, OB and osteocyte apoptosis, fx on OC)
64
** AVN XR finding stages**
0/1 = Normal
2: Osteopenia, cysts (resorption), sclerosis (repair)
3 Subchondral collapse ("crescent sign" w/o articular surface flattening
4 Flattening of articular surface w/o joint space narrowing
5 Flattening of articular surface w/ joint space narrowing and/or acetabular involvement
6 Advanced degenerative changes
65
AVN MRI findings
Line of decreased signal on both T1 and T2
66
AVN bone scan findings
Donut sign: Cold spot (AVN) surrounded by “hot area”
67
AVN Tx
D/C weight bearing x4-8wks
Taper GCs
Analgesia
If reversible (stage 2 or less) → surgery:
-- Core decompression
-- Vascularized fibula grafting
-- Autologous mesenchymal stem cell injxn
Nonreversible (stage 5-6):
--THA
68
Bone marrow edema syndrome (aka transient osteoporosis of the hip) manifestations
Hip pain
-XR= osteopenia
-MRI = bone marrow edema of femoral head AND neck
69
Bone marrow edema syndrome Tx
Bisphosphonate
-Analgesia
-Protective weight bearing
-
-NO CORE DECOMPRESSION
70
Diff between BMES on MRI and AVN
BMES involves femoral head AND femoral neck
71
**HPOA clinical findings**
-Clubbing
-Skin hypertrophy (pachyderma)
-Coarse facial features
Glandular enlargement:
-Dandruff
-Hyperhidrosis
72
**HPOA XR and synovial fluid **
- Periostitis and Periostosis (bone deposition on periosteum) of tubular bones
- Acroosteolysis
-Noninflammatory synovial fluid
73
**HPOA secondary causes**
Lung:
- Cancer (SCC, NSCLC), mets, pleural fibroma
- Cystic fibrosis
- Chronic lung infections, lung abscess
- Mesothelioma
- Bronchiectasis
GI :
-IBD, celiac, PBC
- Cancer: hepatic, GI, POEMS
- HCC, Cirrhosis,
- Whipple,
Other associated:
- Chronic infection - lung, endocarditis, HIV
- Cyanotic congenital heart disease
- Grave’s disease
- Drugs: voriconazole
74
** Give 4 different approaches to minimize GIOP **
Weight bearing exercise
-Vitamin D 1000U/d
-Calcium 1200mgd
-Bisphosphonate
-BMD at baseline then q1-2 until off
-Use lowest dose of GC possible
75
** OP Pathophys - Pro and Anti bone formation players**
Interruption of normal homeostasis of bone turnover causing deterioration of microarchitecture, low bone mass, and fragility fracture risk
Anti-bone formation: RANKL, MCSF, Frz, Sclerostin, DKK-1, continuous PTH
Pro-bone formation: OPG, Wnt, LRP5/6, B Catenin, estrogen/SERM, intermittent PTH
76
Role of RANKL, OPG , Wnt/B catenin
RANKL on OB/activated T cells bind RANK on OC precursors to cause OC differentiation/activation.
- Stimulated by steroids, vit D, OTH, IL1/7/17, TNFa
OPG (cytokine secreted by OB) competitively bind RANKL to prevent RANK binding
Wnt/B-catenin stimulates osteoblasts.
- Frz protein binds/neutralizes Wnt
- Sclerostin & Dickkopf proteins (produced by osteocytes) and block Wnt and OPG
77
** Effect of estrogen on osteoporosis or MoA of SERM/HRT*
Binds E2-R to produce OPG competes w/ RANKL for RANK binding --> less OC differentiation
Inhib Sclerostin (usually inhibits Wnt for OB differentiation)
78
** List 4 zones of cartilage and describe the organization of collagen in each.**
1. **Superficial** - thin collagen fibers parallel to subchondral bone
2. **Middle** zone -collagen fibers = radial bundles.
3. **Deep** zone - largest collagen fibers perpendicular to subchondral bone.
4. **Calcified** zone - collagen fibers penetrate and anchor cartilage to bone
79
** What is the role of RANKL in periarticular osteopenia in RA. Name cells which express RANKL in the joint. **
OB and T cells express RANKL
Periarticular osteopenia 2/2 local production of PGE2, TNFa, IL1 causing increase in RANKL
80
** What is the role of anti TNF in bone formation?**
TNF **increases DKK1 and RANKL to inhibit WNT** (osteoblastogenesis) and induces osteoclastogenesis
Theory that TNF decreases bone formation, so TNFi may increased damage in Ank Spond is unsubstantiated.
81
** Calcitriol or vit D mech of action in OP**
Physiologic levels
- Binds vitamin D receptor on OB to stimulate RANKL (OC differentation) to release Ca from bone to blood
- In bowel, interaction causes Ca-binding protein expression to promote Ca absorption from gut
Pharmacologic levels
- Inhib bone resorption at higher rate than bone formation
82
** Discuss the role of Vit D other than its role in the skeletal system?**
Parathyroid: vit D prevents parathyroid hyperplasia
Heart: deficiency can cause CVD and cardiomyopathy
Immunity: Decreases DC maturation and activation of T cells
Diabetes: vit D deficiency assocd w/ insulin resistance
Cancer: block cell cycle, repair DNA damage, inhib mets, induce apoptosis,
83
** Hormones of bone metabolism **
Ca regulating hormones: PTH, calcitriol, calcitonin
Sex hormones: estrogen
Systemic hormones: GH, Insulin like growth factor, Thryoid hormone, Cortisol
84
** Hormones of bone metabolism: PTH
-Site and mechanism of action**
Acts on kidney to conserve Ca and stimulate calcitriol production
Increases intestinal absorption of Ca
Increase release of Ca from bone to blood
85
** Hormones of bone metabolism: Calcitriol (active vitamin D)
-Site and mechanism of action**
-Increase intestinal absorption of Ca and PO4
-Also acts at kidney and bone level to increase Ca levels
86
** Hormones of bone metabolism: Calcitonin
-Site and mechanism of action**
Produced by thyroid to DECREASE Ca lvls:
* Decreases renal reabsorption of Ca and PO4
* Transiently inactivate OC to prevent resorption
87
** Hormones of bone metabolism: Testosterone
-Site and mechanism of action**
Converted to estrogen in fat cells
88
WHO Definition of normal BMD, vs osteopenia, vs OP
Normal BMD if T score >-1
Osteopenia if T score between -1 and -2.4
OP if T score -2.5 or less
89
** Entry criteria for FRAX **
Drug naiive patients
>40 yo
Osteopenia on BMD
NO fragility #
90
** Osteoporosis of the hip:
3 metabolic causes?
3 structural causes? **
Metabolic cause
- Primary hyperparathyroidism
- Hyperthyroidism
- CKD
- Estrogen deficiency
Structural cause
- Immobilization (eg. astronauts, spinal cord injury, hemiplegia)
- Transient osteoporosis of the hip
- RA affecting hip joint leading to relative disuse
91
**Who should be screened for OP? **
Postmenopausal females & males 50-64 w/ previous # or ≥2 RF
Age 65-69 if 1 RF
Age ≥70 if NO RF
92
** Definition of fragility fracture **
Fracture sustained from force similar to a fall from a standing position or less that would not have occurred in healthy bone, (excludes skull, C spine, face, hands, knees, feet, ankles)
93
How much calcium and vitamin D supplementation is recommended for a 70-year-old Canadian woman?
-Vitamin D 400U/d + vitamin D rich foods
-Calcium 1000mg (1200mg for F) /d from diet
94
Risk factors for vitamin D insufficiency
- Malabsorption: IBD, celiac, bariatric/ gastrectomy
- Reduced skin synthesis (e.g. limited sun, skin pigmentation)
- Liver failure/cirrhosis
- CKD, Nephrotic syndrome
- Meds affecting vit D metab (AED, GC, HAART)
- Hypo/HyperPTH
95
** Pros/Cons SERM (eg raloxifene) over HRT? **
PRO
- LESS risk of invasive breast cancer, endometrial Ca, or cardiovascular event
Cons
- Only works in vertebral #
- Increased VTE
96
**Pros/Cons conventional HRT over raloxifene? **
PROS
- **More potent** anti-resorptive than raloxifene
- **Reduction in hip fracture**
- **Treats vasomotor symptoms** of menopause (raloxifene can cause hot flashes)
Cons
- Concern for CVD and endometrial cancer
97
**Indications for PTH treatment**
aka Teriparatide
- Post-menopausal women with very high fracture risk, particularly those with vertebral fractures
- Severe OP T score <-3.5 w/o # or <2.5+fragility #
- Unable to tolerate BP or failed other therapies
- AFF
- Pregnancy
- Glucocorticoid-induced osteoporosis
98
** Bone markers of formation & loss **
Formation
- ALP,
- Osteocalcin,
- P1NP
Loss
- Serum C-telopeptides (CTX)
- Urine or serum N-telopeptides (NTX)
99
**Utility of following bone markers**
1) Monitor adherence or Tx response
2) Secondary causes of OP
3) Predict who will benefit from rx
4) Surrogate for fractures in clinical trials
100
** GIOP when does it occur and Tx**
Within 3-6mo (peak in 1st 3mo) with ongoing loss per year after
Tx: BP, Ca, vit D for duration of GC
101
**AFF DDX **
Meralgia paresthetica,
GT bursitis,
Hip OA,
AVN,
Bone met
102
**What are the risk factors for osteoporosis in AS?**
OP RF:
- Female,
- Age,
- Post menopausal
- Low BMI,
- Prednisone
Inflammation:
- Disease duration,
- High BASMI
- High ESR/CRP
- Syndesmophytes
103
** Romosozumab black box warning **
Increased risk of MI, stroke, CVD (EVENITY)
104
** Dose of bisphosphonates for OP vs Paget**
Preventing OP:
Zoledronic acid 5mg yearly (treatment or GIOP) or q2y (prevention)
Alendronate 35mg weekly or 5mg daily (double it if GIOP or treating OP )
Risedronate 35mg weekly or 5mg daily
Paget:
Zoledronic acid 5mg once (can repeat if relapse)
Alendronate 40mg daily x6mo
Risedronate 30mg daily x2mo
105
** Periostitis DDX**
- Infection: osteomyelitis, syphilis
- Malignancy: HPOA, Leukemia, lymphoma, Langerhans cell histiocytosis, bone Ca, mets
- Inflammatory: Psoriatic arthritis, reactive arthritis, vasculitis
- Metabolic: thyroid acropachy, acromegaly, scurvy, vitamin A or fluoride toxicity
- Drug: voriconazole
- Other: venous insufficiency
106
** Acroosteolysis DDX **
HPOA
Hyperparathyroidism
Psoriatic arthritis
Scleroderma
107
** Differential for sclerosis/collapse of a single vertebral body.**
- Trauma
- Infection (OM)
- Cancer - primary, mets, leukemia
- Osteoporosis
- Osteomalacia
- Paget's disease
- Hyperparathyroid (OFC)
- Osteogenesis imperfecta
108
** Differential diagnosis for erosion/dissolution of the clavicle.**
Bilateral:
- HyperPTH (acromion is normal, but SC joint may be affected)
- RA (outer 3rd of clavicle affected, later on may affect the acromion)
- Psoriatic arthritis
- Scleroderma
- Atraumatic osteolysis (i.e. weightlifters shoulder from repetitive trauma)
- Osteopetrosis
- Genetic conditions
Unilateral:
- RA
- Post-traumatic osteolysis
- Cancer: myeloma, mets
- Osteomyelitis
